346
Br Heart J 1992;68:346-7
Editorial How can myocarditis be diagnosed and should it be treated? Myocarditis remains an enigma. On one hand it is a diagnosis which is suspected clinically when sudden cardiac failure or arrhythmias or both follow a febrile 'flu-like illness. On the other hand, myocarditis has a defined histological appearance with evidence of myocyte damage and a lymphocytic interstitial inflammatory infiltrate. The similarity between this histological picture and acute rejection led naturally to the suggestion that immunosuppression might be a useful treatment.' Regrettably the clinical and pathological facets of the disease often do not coincide, and the reported frequency of a biopsy positive confirmation of the clinical diagnosis has at best been variable. Leaving this difficulty aside it was unclear whether any form of treatment influenced the ultimate outcome. Clinical experience showed that in the short-term some patients recovered spontaneously, others died. Longer term follow up showed that some patients had impaired left ventricular function and some late deaths occurred. Individual clinicians did not see enough cases to assess the impact of steroid or immunosuppressive treatment. A large trial was initiated by Jay Mason at the University of Utah Medical Center to answer specifically the question of whether immunosuppression improved prognosis. A panel of international experts in the histology of myocarditis met in Dallas, and laid down strict criteria for the diagnosis and terminology used in reporting on the biopsy specimens.2 The preliminary results of the trial were reported to the American College of Cardiology meeting in Dallas in April 1992 and were discussed in the ACCEL (American College of Cardiology Extended Learning) programme for May 1992. As its starting point the trial recruited patients with a short history (
Br Heart J 1992;68:346-7
Editorial How can myocarditis be diagnosed and should it be treated? Myocarditis remains an enigma. On one hand it is a diagnosis which is suspected clinically when sudden cardiac failure or arrhythmias or both follow a febrile 'flu-like illness. On the other hand, myocarditis has a defined histological appearance with evidence of myocyte damage and a lymphocytic interstitial inflammatory infiltrate. The similarity between this histological picture and acute rejection led naturally to the suggestion that immunosuppression might be a useful treatment.' Regrettably the clinical and pathological facets of the disease often do not coincide, and the reported frequency of a biopsy positive confirmation of the clinical diagnosis has at best been variable. Leaving this difficulty aside it was unclear whether any form of treatment influenced the ultimate outcome. Clinical experience showed that in the short-term some patients recovered spontaneously, others died. Longer term follow up showed that some patients had impaired left ventricular function and some late deaths occurred. Individual clinicians did not see enough cases to assess the impact of steroid or immunosuppressive treatment. A large trial was initiated by Jay Mason at the University of Utah Medical Center to answer specifically the question of whether immunosuppression improved prognosis. A panel of international experts in the histology of myocarditis met in Dallas, and laid down strict criteria for the diagnosis and terminology used in reporting on the biopsy specimens.2 The preliminary results of the trial were reported to the American College of Cardiology meeting in Dallas in April 1992 and were discussed in the ACCEL (American College of Cardiology Extended Learning) programme for May 1992. As its starting point the trial recruited patients with a short history (
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